miRNAs mediate the impact of smoking on dental pulp stem cells via the p53 pathway
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View abstract on PubMed
Summary
This summary is machine-generated.Cigarette smoke exposure harms dental pulp stem cells' regenerative abilities. Specific microRNAs (miRNAs) regulate cell cycle and p53 pathways, offering potential therapeutic targets for smokers.
Area Of Science
- Stem Cell Biology
- Epigenetics
- Molecular Biology
Background
- Cigarette smoke induces genomic and epigenomic alterations in cells.
- Dental pulp stem cells (DPSCs) possess regenerative potential crucial for tissue repair.
- MicroRNAs (miRNAs) play significant roles in regulating cellular functions and disease pathogenesis.
Purpose Of The Study
- To investigate the biological effects of prolonged cigarette smoke condensate (CSC) exposure on DPSCs.
- To identify the role of miRNAs in mediating CSC-induced changes in DPSC behavior and function.
- To explore potential therapeutic targets for mitigating smoking-related damage to stem cells.
Main Methods
- DPSCs were exposed to varying concentrations of CSC for up to 6 weeks.
- Assessed DPSC proliferation, survival, migration, and differentiation.
- Performed cytokine and miRNA expression profiling, followed by bioinformatic pathway analysis.
Main Results
- Extended CSC exposure significantly impaired DPSC regenerative capacity.
- Altered miRNA profiles were associated with cell cycle, cancer, and key signaling pathways (TNF, TGF-β, p53, PI3K-Akt, mTOR, ErbB).
- Specific miRNAs (has-miR-26a-5p, has-miR-26b-5p, has-miR-29b-3p) were identified as regulators of p53 and cell cycle pathways in DPSCs.
Conclusions
- MiRNAs are critical regulators of DPSC cellular activities affected by cigarette smoke.
- Targeting specific miRNAs presents a promising strategy for modulating stem cell regeneration in smokers.
- Understanding miRNA-mediated pathways in smoking individuals is vital for disease prevention and control.
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